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10.1073/pnas.1718600115 http://scihub22266oqcxt.onion/10.1073/pnas.1718600115 C5798377!5798377!29343648     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2018 ; 115 (5): E982-91 Nephropedia Template TP {{tp|p=29343648|t=2018. PAR1 agonists stimulate APC-like endothelial cytoprotection and confer resistance to thromboinflammatory injury |pdf=|usr=}}{{29343648}} gab.com Text PAR1 agonists stimulate APC-like endothelial cytoprotection and confer resistance to thromboinflammatory injury JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29343648 #FOAvip Protease-activated receptors (PARs) are G-protein?coupled receptors (GPCRs) that are activated by proteolysis and couple to multiple distinct G-proteins. Cleavage of PAR1 in endothelium stimulates either proinflammatory or antiinflammatory signaling depending on the activating protease and is important in thrombosis and inflammation. Yet the biased signaling of PAR1 has made its pharmacological modulation challenging. We show that a family of compounds, parmodulins, acts at the cytosolic face of PAR1 to differentially control G-protein coupling and stimulate cytoprotective signaling while blocking deleterious signaling. Parmodulins are antiinflammatory and antithrombotic in vivo. These compounds demonstrate the utility of targeting the cytosolic face of GPCRs to selectively modulate downstream signaling and could provide an alternative for treatment of thromboinflammatory disorders. Twit Text FOAVip PAR1 agonists stimulate APC-like endothelial cytoprotection and confer resistance to thromboinflammatory injury ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29343648 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29343648 #FOAvip English Wikipedia <ref>{{Cite pmid|29343648}}</ref> PAR1 agonists stimulate APC-like endothelial cytoprotection and confer resistance to thromboinflammatory injury #MMPMID29343648 De Ceunynck K; Peters CG; Jain A; Higgins SJ; Aisiku O; Fitch-Tewfik JL; Chaudhry SA; Dockendorff C; Parikh SM; Ingber DE; Flaumenhaft R Proc Natl Acad Sci U S A 2018[Jan]; 115 (5): E982-91 PMID29343648show ga Protease-activated receptors (PARs) are G-protein?coupled receptors (GPCRs) that are activated by proteolysis and couple to multiple distinct G-proteins. Cleavage of PAR1 in endothelium stimulates either proinflammatory or antiinflammatory signaling depending on the activating protease and is important in thrombosis and inflammation. Yet the biased signaling of PAR1 has made its pharmacological modulation challenging. We show that a family of compounds, parmodulins, acts at the cytosolic face of PAR1 to differentially control G-protein coupling and stimulate cytoprotective signaling while blocking deleterious signaling. Parmodulins are antiinflammatory and antithrombotic in vivo. These compounds demonstrate the utility of targeting the cytosolic face of GPCRs to selectively modulate downstream signaling and could provide an alternative for treatment of thromboinflammatory disorders. äPAR1 agonists stimulate APC-like endothelial cytoprotection and confer(epmc).pdf DeepDyve Pubget Overpricing